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Cancers driven by MYC need to make proteins at an unusually fast rate. Slowing the cell's protein factory hits them harder than it hits normal cells.
MYC amplification imposes dependence on cap-dependent translation, ribosome biogenesis and eIF4A/eIF4E activity. Selective eIF4A inhibitors (for example zotatifin) and RNA polymerase I inhibitors have entered clinical trials. Rather than treating these as broad cytotoxics, the proposal is to select patients by MYC amplification or a translation-dependency signature, which has not been done systematically.
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